MCM5 Activators
The class of MCM5 activators constitutes a multifaceted array of chemicals that intricately regulate the activity of the MCM5 protein, an indispensable component of the MCM complex crucial for the initiation of DNA replication. These activators exert their influence through a spectrum of direct and indirect mechanisms, emphasizing the interconnectedness of cellular processes modulated by these compounds. Direct activators, exemplified by Aphidicolin, operate by directly inhibiting DNA polymerases, thereby inducing replication stress and subsequently activating MCM5. This activation becomes a pivotal component of the cellular response when confronted with challenges in DNA synthesis, underscoring the significance of MCM5 in maintaining genomic stability during critical phases of the cell cycle. Indirect activators, including Gemcitabine and Triptolide, exhibit their effects by disrupting DNA synthesis and transcription, respectively. Gemcitabine incorporates into DNA, inhibiting its synthesis and triggering compensatory mechanisms that involve the activation of MCM5 to overcome obstacles in replication. Triptolide, as a transcriptional inhibitor, disrupts RNA polymerase II function, creating an imbalance in DNA synthesis and prompting the compensatory activation of MCM5.
Moreover, compounds such as Doxorubicin, Camptothecin, and Cisplatin induce DNA damage, setting off a cascade of events leading to the activation of MCM5 to maintain genomic integrity during the replication process. Etoposide, by inhibiting topoisomerase II, causes DNA damage, activating MCM5 as part of the intricate response to repair damaged DNA. Hydroxyurea, Mitomycin C, Topotecan, and Bleomycin, in diverse ways, modulate nucleotide metabolism or induce DNA damage, indirectly activating MCM5 to ensure proper DNA replication under conditions of replication stress. This intricate interplay between MCM5 and these activators underscores the regulatory role of these compounds in modulating key cellular processes and maintaining genomic stability. In summation, the class of MCM5 activators offers a nuanced perspective on the regulatory networks governing DNA replication. Delving into the specific biochemical and cellular pathways influenced by these compounds enhances our understanding of the dynamic processes involved in DNA replication initiation, providing valuable insights into potential avenues for targeted interventions in conditions where DNA replication fidelity is paramount.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $84.00 $306.00 $1104.00 | 30 | |
Aphidicolin is a direct activator of MCM5, functioning by inhibiting DNA polymerase α and δ. This inhibition induces replication stress, leading to the activation of the MCM complex, including MCM5, as part of the cellular response to replication challenges. The increased demand for MCM5 in the replication machinery highlights the direct impact of Aphidicolin on the activation of MCM5 during DNA synthesis. | ||||||
2′-Deoxy-2′,2′-difluorocytidine | 95058-81-4 | sc-275523 sc-275523A | 1 g 5 g | $56.00 $128.00 | ||
2'-Deoxy-2',2'-difluorocytidine indirectly activates MCM5 by incorporating into DNA and inhibiting DNA synthesis. Its incorporation disrupts the normal DNA replication process, triggering compensatory mechanisms that involve the activation of MCM5 to overcome replication obstacles. | ||||||
Triptolide | 38748-32-2 | sc-200122 sc-200122A | 1 mg 5 mg | $90.00 $204.00 | 13 | |
Triptolide indirectly activates MCM5 by inhibiting transcription. As a transcriptional inhibitor, Triptolide disrupts RNA polymerase II function, creating an imbalance in DNA synthesis and triggering the compensatory activation of MCM5. This indirect activation underscores the interconnected nature of transcriptional and replicative processes, emphasizing the role of MCM5 in responding to disruptions in transcriptional machinery induced by Triptolide. | ||||||
Doxorubicin | 23214-92-8 | sc-280681 sc-280681A | 1 mg 5 mg | $176.00 $426.00 | 43 | |
Doxorubicin indirectly activates MCM5 by inducing DNA damage and inhibiting DNA topoisomerases. The resulting DNA lesions lead to the activation of the MCM complex, including MCM5, as part of the cellular response to repair damaged DNA. This indirect activation highlights the link between DNA damage response pathways and the compensatory activation of MCM5 to ensure the fidelity of DNA replication and maintain genomic stability during the presence of genotoxic stress. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $58.00 $186.00 $94.00 | 21 | |
Camptothecin indirectly activates MCM5 by inhibiting DNA topoisomerase I. Its inhibition induces DNA damage and triggers the activation of MCM5 as a response to maintain genomic integrity during replication. This indirect activation illustrates the regulatory role of Camptothecin in modulating the dynamics of DNA replication and the compensatory activation of MCM5 to ensure proper DNA synthesis in the presence of topoisomerase I inhibition. | ||||||
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $138.00 $380.00 | 101 | |
Cisplatin indirectly activates MCM5 by inducing DNA crosslinks and DNA damage. The resulting DNA lesions activate the MCM complex, including MCM5, as part of the cellular response to repair damaged DNA. This indirect activation underscores the interplay between DNA damage response pathways and the compensatory activation of MCM5 to maintain genomic stability and ensure the fidelity of DNA replication during exposure to DNA-damaging agents such as Cisplatin. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $51.00 $231.00 $523.00 | 63 | |
Etoposide indirectly activates MCM5 by inducing DNA damage and inhibiting topoisomerase II. The DNA lesions generated activate the MCM complex, including MCM5, as part of the cellular response to repair damaged DNA. This indirect activation emphasizes the link between DNA damage response pathways and the compensatory activation of MCM5 to maintain genomic stability and ensure proper DNA replication during exposure to genotoxic stress induced by Etoposide. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $78.00 $260.00 | 18 | |
Hydroxyurea indirectly activates MCM5 by inhibiting ribonucleotide reductase, leading to decreased nucleotide pools and replication stress. The resulting imbalance in nucleotide availability activates the MCM complex, including MCM5, to overcome replication challenges. | ||||||
Mitomycin C | 50-07-7 | sc-3514A sc-3514 sc-3514B | 2 mg 5 mg 10 mg | $66.00 $101.00 $143.00 | 85 | |
Mitomycin C indirectly activates MCM5 by inducing DNA crosslinks and damage. The resulting DNA lesions activate the MCM complex, including MCM5, as part of the cellular response to repair damaged DNA. This indirect activation underscores the interconnectedness between DNA damage response pathways and the compensatory activation of MCM5 to ensure genomic stability and fidelity during exposure to DNA-damaging agents like Mitomycin C. | ||||||
Topotecan | 123948-87-8 | sc-338718 | 100 mg | $582.00 | ||
Topotecan indirectly activates MCM5 by inhibiting DNA topoisomerase I. The inhibition induces DNA damage, triggering the activation of the MCM complex, including MCM5, as part of the cellular response to repair damaged DNA. This indirect activation emphasizes the regulatory role of Topotecan in modulating topoisomerase I activity and the compensatory activation of MCM5 to maintain genomic integrity and proper DNA replication under conditions of topoisomerase I inhibition. | ||||||